1. Field of the Invention
This invention relates generally to medicine and more specifically to improved cardiac pacing systems including methods of pacing and sensing in the treatment of patients with cardiac disease.
2. Description of the Prior Art
Artificial cardiac pacemakers are electrical devices employed to electrically stimulate the heart in the absence of intrinsic cardiac electrical activity. They are currently used to treat a wide range of cardiac arrhythmias and are either implanted or used temporarily in the care of over 300,000 patients annually worldwide. Their ability to maintain life in the treatment of various arrhythmias when operating reliably is widely recognized.
Recent progress in pacemaker design has addressed improving the quality of recipients, lives with the advent of new pacing modes. Modern pacemakers may pace and sense in one or both chambers (atrial and ventricular) of the heart and may deliver electrical stimuli to the heart's chambers in the absence of intrinsic activity above a preset, atrial tracking or sensor indicated rate according to various pacing modes. These modern pacing modes are employed to produce atrio-ventricular (A-V) synchrony and/or rate increases based on various sensor inputs with the intention of increasing the exercise tolerance of pacemaker recipients and, increasing the cardiac output of pacemaker recipients during various additional physiologic states. There is debate surrounding the choice of an appropriate pacing mode for an individual patient due to the fact that rate increases are not tolerated by certain patients and are not beneficial to others. The development of atrial arrhythmias, the technical difficulties of placing an atrial lead, and the poor long term performance of certain atrial leads discourage certain doctors from dual chamber use.
An important similarity exists in all current pacemaker systems regardless of the available modes they employ. Current pacemaker systems stimulate and sense individual cardiac chambers through single pacing and sensing foci that may operate through bipolar or unipolar electrical pathways depending upon certain programmed parameters. These single focus pacemakers will be termed conventional pacemakers for the purpose of the analysis hereinafter described. Conventional pacemakers produce major differences in electrocardiographic recordings during pacing when compared to normal sinus rhythm.
An electrocardiogram or EKG is a recording of the electrical activity of the heart obtained from electrodes placed on the skin surface of a patient at various locations. An EKG recording from lead II displays this activity as recorded from electrodes placed on the right arm and left leg of a patient. FIG. 1a illustrates a normal sinus rhythm lead II EKG with a conventional ventricular paced lead II EKG shown in FIG. 1b, both shown with the same time scale and identical ventricular rates in the same patient under identical physiologic conditions other than pacing. A normal EKG generally consists of six major deflections or waves which are referred to as P, Q, R, S, T and U waves. When an individual heart muscle cell is activated, or fired, initiating its contraction, it gives off a characteristic electrical signal which is termed an action potential. Depolarization or activation is defined as the excursion of the action potential from the resting potential of the cell and repolarization is defined as the return of the action potential to the resting potential of the cell. Therefore a P wave describes the electrical activity of the atrial muscle cells as they depolarize, the QRS complex describes the electrical activity of the ventricular muscle cells as they depolarize (or activate) and the T wave describes the electrical activity of the ventricular muscle cells as they repolarize, as recorded from surface electrodes. U waves are not important for this analysis and are not shown or discussed for this reason.
In FIG. 1b the vertical line that begins the conventionally paced QRS complex represents a pacemaker spike which is an electrical impulse that initiates ventricular depolarization. Ventricular depolarization and then ventricular repolarization follow and will be referred to as a conventionally paced QRS complex and conventionally paced T wave respectively. As shown in FIGS. 1a and 1b, conventionally paced QRS complexes generally produce an opposite direction of deflection as compared to a normal QRS when recorded from lead II. P waves are not shown in the paced EKG due to the fact that they may or may not be present, or may be present in synchrony with the paced ventricular complex depending upon the pacing mode employed and the patient's intrinsic atrial rhythm.
Normal EKG morphologies and durations are variable from patient to patient and may vary significantly from normal in the presence of heart disease. FIGS. 1a and 1b represent EKG morphologies which are illustrative of commonly encountered recordings as supported by the literature. The analysis hereinafter described deals with the comparison of interval durations that are important to ventricular function and provides valid comparisons between paced and intrinsic ventricular complexes regardless of the exact EKG morphology recorded from an individual patient. These comparisons are also supported by the literature.
The following comparisons of interval durations will be made using a hypothetical patient whose chosen normal sinus and conventionally paced EKGs are illustrated in FIGS. 1a and 1b respectively. Therefore all firing times and durations noted will be referred to as distinctly describing this particular patient, with the realization that these durations may vary from patient to patient. Examples of durations obtainable by ventricular sequential pacing will be made in the same patient and incorporate specific assumptions producing durations that will similarly be referred to as distinctly describing this particular patient, with the realization that these durations may vary from patient to patient.
FIGS. 1a and 1b illustrate three major differences between normal sinus rhythm and conventional ventricular paced EKG morphologies. The Q-T interval, defined as the interval from the initiation of the Q wave to the termination of the T wave, is substantially shorter in normal sinus rhythm as shown in FIG. 1a than in a conventionally paced rhythm as depicted by a commonly encountered Q-Tns (normal sinus) of 250 msec compared to a Q-Tcp (conventionally paced) of 350 msec as shown in FIG. 1b. Secondly, the ST segment, defined as the interval from the end of the S wave to the beginning of the T wave, a period of normally little electrical activity, is evident in the normal EKG but not in the conventionally paced EKG. The ST segment is a valuable tool for cardiologists in the diagnosis of ischemic heart disease. Thirdly, the duration of the QRS complex, defined from the initiation of the Q wave to the termination of the S wave, representing ventricular depolarization, is shorter in a normal EKG as depicted by a QRSns of 50 msec compared to a QRScp of 150 msec in a conventionally paced EKG.
Therefore; EQU (Q-Tcp)-(Q-Tns)=(QRScp)-(QRSns)=100 msec
where ns=normal sinus and cp=conventionally paced.
Systole is defined as the period of time that the ventricles are contracting. Electromechanical systole is defined as the period from initial electrical activation of ventricular muscle to the end of contraction which, closely approximates the Q-T interval. Electromechanical systole will hereinafter be referred to as systole or the systolic interval and systole will be considered equal to the Q-T interval. Diastole or the diastolic interval is defined as the period of time that the ventricles relax and for the purposes of the following analysis is the period of time when the ventricles are not in systole. The RI (rate interval) shown in FIGS. 1a and 1b is 500 msec which is equivalent to a ventricular rate of 120 beats per minute. It should be understood that the principles of the hereinafter analysis will apply at any other rate chosen.
The percentage of time that the ventricles contract or percent systole is defined as the ratio of Q-Tns to RI in normal sinus rhythm and Q-Tcp to RI in a conventionally paced rhythm.
Therefore; ##EQU1##
The percentage of time that the ventricles relax is defined as percent diastole as shown below; ##EQU2##
Percent systole is an extremely important determinant of ventricular function. The lower the percent systole the more forceful a ventricular contraction is produced due to the fact that the ventricular muscle fibers contract to produce a more rapid ejection of blood from the heart as compared to higher percent systoles. This is referred to in the art as an element of increased ventricular contractility. Thus, as percentage systole decreases, increases in the efficiency of ventricular contraction, stroke volume and ejection fraction are realized. Lowering the percent systole also decreases the duration of time during which pressure is applied to the coronary arteries. Greater percent systoles produce local intramural forces of contraction around the coronary arteries that are applied over a longer period of time, accordingly decreasing coronary perfusion during exercise and in the resting state.
As seen in the above formulas, as percent systole increases, percent diastole decreases. The great majority of exercise related coronary blood flow increase occurs during diastole. Accordingly, decreases in percent diastole produce significant decreases in coronary blood flow during exercise and significant but less dramatic decreases in coronary blood flow in the resting state. The time available for ventricular filling is equal to the diastolic interval. Ventricular filling time is increased with increased percent diastoles, accordingly increasing cardiac output by increasing stroke volume and ventricular preload. Electrically, the longer the Q-T interval the greater the ventricular muscle's vulnerable period during repolarization and the more likely it becomes for a patient to develop further arrhythmias.
Q-T interval is therefore an extremely important determinant of ventricular function during exercise as well as in the resting state. Conventional pacemakers produce significant Q-T interval prolongation with consequent decreases in ventricular contractility, cardiac output, coronary blood flow and electrical stability of the ventricular muscle. A pacemaker system that provides the ability to shorten the Q-T interval during pacing would significantly improve the ventricular function of pacemaker recipients. These improvements would be applicable to all current and future pacing modes employed and would improve the quality of life of pacemaker recipients in the resting state, during exercise and under various additional physiologic circumstances.